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Energy recovery ventilation plays a crucial role in providing fresh air and managing respiratory diseases, such as COVID-19. This study focuses on the computational fluid dynamics (CFD) analysis of a compact heat exchanger within a heat recovery ventilator and discusses the findings. However, conducting such an analysis is challenging due to the complex nature of the desired modules, which include intricate fin geometry and the combination of crossflow and counterflow regions in a compact heat exchanger, requiring extensive computational resources. To overcome these limitations, the entire model is treated as a computable unit cell, and the complex calculations involving crossflow and counterflow are simplified by summing individual simulations for each flow type. Furthermore, the detailed numerical modeling method is compared with experimental results, demonstrating the utility of the proposed CFD modeling approach for analyzing plate–fin compact heat exchangers. [ABSTRACT FROM AUTHOR]

Abstract: Platelet-activating factor (PAF), a potent mediator of inflammatory and immune responses, plays various roles in neuronal functions. However, little is known about the role of PAF/platelet-activating factor receptor (PAF-R) in Parkinson’s disease. Treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) resulted in significant increases in PAF species in the striatum of wild-type mice. These increases paralleled PAF-R gene expression in wild-type mice. Although nuclear factor kappa B (NF-κB) DNA-binding activity was increased significantly in MPTP-treated wild-type mice, this increase was not significant in PAF-R antagonist ginkgolide B (GB)-treated mice or PAF-R knockout (PAF-R−/−) mice. Pyrrolidine dithiocarbamate (PDTC), an NF-κB inhibitor, significantly ameliorated the dopaminergic deficits induced by MPTP in wild-type mice. MPTP treatment significantly increased oxidative damage, the immunoreactivity of ionized calcium binding adaptor molecule 1 (Iba-1)-positive microglial cells, and microglial differentiation of the M1 type in the striatum of wild-type mice. Consistently, PDTC significantly attenuated MPTP-induced behavioral impairments in wild-type mice. However, dopaminergic deficits, oxidative damage, reactive microglial cells, and behavioral impairments induced by MPTP were not significantly observed in GB-treated mice or PAF-R−/− mice. PDTC did not significantly alter the attenuations evident in MPTP-treated PAF-R−/− mice, indicating that NF-κB is a critical target for neurotoxic modulation of PAF-R. We propose for the first time that PAF/PAF-R can mediate dopaminergic degeneration via an NF-κB-dependent signaling process. [Copyright &y& Elsevier]

Abstract: We previously reported that interleukin (IL)-6 deficiency potentiates trimethyltin (TMT)-induced convulsive neurotoxicity. The purpose in this study was to investigate the molecular mechanism by which cytokines affect TMT-induced cognitive impairment. To accomplish this, we examined hippocampal changes in Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling in relation to cholinergic parameters after TMT treatment in mice genetically deficient in IL-6 (IL-6−/−), tumor necrosis factor-α (TNF-α−/−), or interferon-γ (IFN-γ−/−). The IL-6−/− mice were the most susceptible to TMT-induced cognitive dysfunction and exhibited significant decreases in JAK2/STAT3 signaling and M1 muscarinic acetylcholine receptor (mAChR) expression, as well as other cholinergic parameters, compared with wild-type (WT) animals. Recombinant IL-6 protein (rIL-6) significantly attenuated these impairments in TMT-treated IL-6−/− mice, whereas an IL-6 receptor antibody potentiated these impairments in TMT-treated WT animals. Inhibition of JAK2 with AG490 or inhibition of cholinergic signaling with the M1 mAChR antagonist dicyclomine counteracted the attenuating effects of rIL-6 on phosphorylated extracellular signal-regulated kinase (ERK) expression, or on cognitive impairment in TMT-treated IL-6−/− mice. However, neither AG490 nor dicyclomine significantly attenuated effects of rIL-6 on acetylcholinesterase values. Our results suggest that activation of JAK2/STAT3 signaling and upregulation of the M1 mAChR are essential components of IL-6-mediated memory improvement against TMT toxicity. [Copyright &y& Elsevier]

Dysphagia associated with Parkinson's disease (PD) affects the mortality and quality of life of patients with PD. Avoiding aspiration and maintaining swallowing ability are among the concerns regarding PD care. Therefore, we developed a swallowing supplement for easier swallowing and tolerability in patients with PD. Thirty patients with PD and 50 healthy controls were enrolled and their swallowing function measured using the videofluoroscopic swallowing study (VFSS) and several dysphagia scales. The Unified Parkinson's Disease Rating Scale motor scores, Hoehn and Yahr stage, and levodopa doses were evaluated in patients with PD. The VFSS and survey were used to assess the viscosity, color, taste, nutrition, safety, and tolerability of the swallowing supplement. The MMSE score, serum albumin, and hemoglobin levels, and oral conditions were worse in the PD group than in the control group. Compared with controls, patients with PD had significantly lower total and sub-item scores of the swallowing quality of life (swal-QoL). Using commercialized yogurt, the pharyngeal delay time (PDT) and the modified penetration aspiration scale were higher in the PD group than in the control group. The swallowing supplement significantly shortened the PDT and pharyngeal transit time (PTT). Moreover, compared with commercialized yogurt, it improved pharyngeal wall coating, PTT, and aspiration in the videofluoroscopic dysphagia subscales. The survey scores were above average to good in the "easy swallowing" and "pharyngeal residual sense" items and tolerable in the remaining 6 preference items. This swallowing supplement could prevent aspiration and dysphagia complications in patients with PD. [ABSTRACT FROM AUTHOR]